In the conditioned suppression of drinking (CSD) conflict model of anxiety, four (4) clinically effective yet distinct anxiolytic treatments have been shown to exert robust anticonflict effects; (1) acute benzodiazepine or barbiturate treatment, (2) acute buspirone challenges following chronic buspirone treatment, (3) chronic antidepressant treatment and (4) chronic clonidine treatment. The present studies are designed to investigate possible behavioral, neuroanatomical and neurotransmitter mechanisms for the anticonflict action of these diverse anxiolytic treatments. Studies in Specific Aim 1 ar designed to test the validity of the hypothesis that the anticonflict effect of the above-mentioned treatments, as measured in the CSD conflict paradigm, are in fact a reflection of their anxiolytic actions. First, the effects of these anxiolytic treatments will be determined (in some cased, redetermined) in the elevated plus maze conflict task, a non-shock conflict task which has been extensively validated as an animal model for anxiety. Second, shock sensitivity testing following the various anxiolytic treatments will be conducted to confirm that the anticonflict effects observed in the CSD procedure are not secondary to antinociceptive effects. Studies in Specific Aim 2 will determine the importance of two limbic sites (central nucleus of the amygdala [CNA} and lateral septum [LS]) for the expression of the various anxiolytic treatment effects. In these studies, the effects of these anxiolytic treatments will be determined following electrolytic lesions of either the CNA, LS or both structures. Studies in Specific Aim 3 will determine the importance of the monoamine neurotransmitters norepinephrine (NE) and 5-hydroxytryptamine (5HT) for the expression of the anticonflict effects of the various treatments. In these studies, the effects of the anxiolytic treatments will be determined following chemical (6-OHDA, 5,7-DHT) or electrolytic lesions of NE-containing neurons in the locus ceruleus (LC), 5HT-containing neurons within the dorsal raphe nucleus (DRN), or neurons in both sites. Together, the proposed studies will address the neuroanatomical and neurotransmitter mechanisms underlying the expression of a diverse group of anxiolytic treatments.